Nature article

"private" wrote:
> I am really interested in the field and plan on reading the article.
It is available at www.nature.com even to non-subscribers. The site
is rather busy right now :-)
> what does the p stand for in p66shc? does it mean protein?
Yes. Scandalously unimaginative, but common.
> does that mean the serine phosphorylase is promoting or blocking
> p66shc?
Promoting. Well, activating.
> is this good or bad for extending life span?
It's the normal ("wild-type") state, so one can't meaningfully say
whether it's good or bad for something abnormal (extending life span).
We can only ask: "is inactivation of the serine phosphorylation good
or bad for extending lifespan?", and the answer is "good, apparently".
> I thought apotosis was good for getting rid of damaged cells? How
> would resisting apotosis extend life span?
Quite right. That was the logic that led me to the proposal stated in
my previous post - that loss of apotosis is bad and forces the body to
up-regulate other things that make that apoptosis less necessary. I'm
quite sure that this would not work if ALL apoptosis were abolished,
since apoptosis is crucial for many aspects of development, but what's
being studied here is the specific inhibition only of stress-induced
apoptosis, which may be a different matter.
> Is the normal stress response good or bad for extending life span?
See above -- it's not rigorous to talk about something normal as being
good or bad for something that isn't normal, e.g. extending life span.
> I thought these mice had improved stress response?
Yes, perhaps due to over-compensation by some (as yet unidentified)
parts of the stress management arsenal for impairment of another part.
Aubrey de Grey